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Archives of Cardiovascular Diseases 2017Pulmonary hypertension due to left heart disease, also known as group 2 pulmonary hypertension according to the European Society of Cardiology/European Respiratory... (Review)
Review
Pulmonary hypertension due to left heart disease, also known as group 2 pulmonary hypertension according to the European Society of Cardiology/European Respiratory Society classification, is the most common cause of pulmonary hypertension. In patients with left heart disease, the development of pulmonary hypertension favours right heart dysfunction, which has a major impact on disease severity and outcome. Over the past few years, this condition has been considered more frequently. However, epidemiological studies of group 2 pulmonary hypertension are less exhaustive than studies of other causes of pulmonary hypertension. In group 2 patients, pulmonary hypertension may be caused by an isolated increase in left-sided filling pressures or by a combination of this condition with increased pulmonary vascular resistance, with an abnormally high pressure gradient between arteries and pulmonary veins. A better understanding of the conditions underlying pulmonary hypertension is of key importance to establish a comprehensive diagnosis, leading to an adapted treatment to reduce heart failure morbidity and mortality. In this review, epidemiology, mechanisms and diagnostic approaches are reviewed; then, treatment options and future approaches are considered.
Topics: Heart Failure; Humans; Hypertension, Pulmonary; Predictive Value of Tests; Prognosis; Risk Factors; Stroke Volume; Ventricular Dysfunction, Left; Ventricular Dysfunction, Right; Ventricular Function, Left; Ventricular Function, Right; Ventricular Pressure
PubMed: 28411107
DOI: 10.1016/j.acvd.2017.01.010 -
Expert Review of Cardiovascular Therapy Feb 2008While the debate continues regarding the role of polymorphisms of beta(1)-adrenoceptors on the clinical outcomes and beneficial effects of beta-blockers in patients with...
While the debate continues regarding the role of polymorphisms of beta(1)-adrenoceptors on the clinical outcomes and beneficial effects of beta-blockers in patients with heart failure, we need to step back and examine the evidence in the peer-reviewed literature more closely.
Topics: Adrenergic beta-Antagonists; Humans; Polymorphism, Genetic; Receptors, Adrenergic, beta-1; Treatment Outcome; Ventricular Dysfunction
PubMed: 18248268
DOI: 10.1586/14779072.6.2.145 -
Heart (British Cardiac Society) Aug 2011
Review
Topics: Cardiovascular Diseases; Echocardiography, Doppler; Heart Ventricles; Humans; Prognosis; Ventricular Dysfunction; Ventricular Function, Left; Ventricular Function, Right
PubMed: 21775511
DOI: 10.1136/hrt.2009.184390 -
International Journal of Cardiology Mar 2014
Topics: Acute Disease; Animals; Disease Models, Animal; Humans; Pulmonary Embolism; Rats; Takotsubo Cardiomyopathy; Ventricular Dysfunction, Right
PubMed: 24447755
DOI: 10.1016/j.ijcard.2013.12.297 -
Herz Apr 2015
Topics: Heart Failure; Humans; Ventricular Dysfunction, Left
PubMed: 25822418
DOI: 10.1007/s00059-015-4212-8 -
Circulation. Cardiovascular Imaging May 2017
Review
Topics: Blalock-Taussig Procedure; Clinical Decision-Making; Disease Progression; Echocardiography, Doppler, Color; Electrocardiography; Exercise Tolerance; Female; Heart Failure; Hemodynamics; Humans; Magnetic Resonance Imaging; Middle Aged; Predictive Value of Tests; Prognosis; Tetralogy of Fallot; Tomography, X-Ray Computed; Ventricular Dysfunction, Left; Ventricular Dysfunction, Right; Ventricular Function, Left; Ventricular Function, Right
PubMed: 28495821
DOI: 10.1161/CIRCIMAGING.116.004270 -
The American Journal of Cardiology Oct 2009
Topics: Angiography; Diagnosis, Differential; Heart Ventricles; Humans; Takotsubo Cardiomyopathy; Ventricular Dysfunction, Left
PubMed: 19801043
DOI: 10.1016/j.amjcard.2009.07.030 -
Expert Opinion on Pharmacotherapy Jun 2001This review focuses on diastolic dysfunction with special emphasis on isolated diastolic dysfunction where impairment in diastolic function occurs in the absence of... (Review)
Review
This review focuses on diastolic dysfunction with special emphasis on isolated diastolic dysfunction where impairment in diastolic function occurs in the absence of concomitant reduction in systolic function. The phenomena which influence diastolic function, the clinical spectrum of diastolic dysfunction, the physiological perturbations which may serve as therapeutic targets for pharmacological therapy and recent therapeutic trials are reviewed. Recommendations regarding the therapeutic approach to the patient with diastolic dysfunction are summarised.
Topics: Animals; Clinical Trials as Topic; Coronary Disease; Diastole; Guidelines as Topic; Heart Failure; Humans; Stroke Volume; Ventricular Dysfunction
PubMed: 11585015
DOI: 10.1517/14656566.2.6.997 -
The American Journal of Cardiology Jan 2022Many Fontan patients with and without systolic ventricular dysfunction are being treated with angiotensin-converting enzyme (ACE) inhibitors, despite its effectiveness...
Many Fontan patients with and without systolic ventricular dysfunction are being treated with angiotensin-converting enzyme (ACE) inhibitors, despite its effectiveness remaining unclear. In the present study, we evaluated the short-term effect of enalapril on exercise capacity, vascular and ventricular function in pediatric Fontan patients with moderate-good systolic ventricular function. Fontan patients between 8 and 18 years with moderate-good systolic ventricular function and without previous ACE inhibitor treatment were included and were treated with enalapril for 3 months. During the first 2 weeks, the dosage was titrated according to systolic blood pressure (SBP). Exercise tests, ventricular function assessed by echocardiography, arterial stiffness measurements, and plasma levels of N-terminal pro-B-type natriuretic peptide assessed before and after a 3-month enalapril treatment period was compared. A total of 28 Fontan patients (median age 13.9 years, 6 to 15 years after Fontan operation) completed the study with a mean dosage of 0.3 ± 0.1 mg/kg/d. A total of 6 patients (21%) experienced a significant drop in SBP and 6 others (21%) experienced other adverse events. Enalapril treatment lowered the SBP (from 110 to 104 mmHg, p = 0.003) and levels of N-terminal pro-B-type natriuretic peptide (from 80 to 72 ng/L, p = 0.036). However, enalapril treatment did not improve exercise capacity, ventricular function, or arterial stiffness. In conclusion, short-term ACE inhibition has no beneficial effect in Fontan patients with moderate-good systolic ventricular function.
Topics: Adolescent; Angiotensin-Converting Enzyme Inhibitors; Blood Pressure; Child; Echocardiography; Enalapril; Exercise Test; Exercise Tolerance; Female; Fontan Procedure; Humans; Hypotension; Male; Natriuretic Peptide, Brain; Peptide Fragments; Systole; Treatment Outcome; Vascular Stiffness; Ventricular Dysfunction
PubMed: 34774285
DOI: 10.1016/j.amjcard.2021.10.013 -
The American Journal of Cardiology Mar 2006The pathophysiologic mechanisms of left ventricular (LV) dysfunction in isolated ventricular noncompaction (IVNC) remain unclear. Evaluating global and segmental... (Comparative Study)
Comparative Study
The pathophysiologic mechanisms of left ventricular (LV) dysfunction in isolated ventricular noncompaction (IVNC) remain unclear. Evaluating global and segmental systolic LV function in 65 patients with IVNC, this study found that normal wall motion was more common in noncompacted than in compacted segments. The number of noncompacted segments per patient correlated positively with the LV ejection fraction and negatively with LV end-diastolic volume index. These paradoxical findings support the concept that noncompaction represents a marker of a more generalized (cardio)myopathy rather than the direct pathophysiologic substrate of this still little-understood disease.
Topics: Adult; Echocardiography, Doppler, Color; Female; Humans; Male; Middle Aged; Observer Variation; Stroke Volume; Ventricular Dysfunction, Left
PubMed: 16490448
DOI: 10.1016/j.amjcard.2005.09.109